Title of article :
Maté attenuates DNA damage and carcinogenesis induced by diethylnitrosamine and thermal injury in rat esophagus
Author/Authors :
Silva، نويسنده , , Juliana Ferreira da and Bidinotto، نويسنده , , Lucas Tadeu and Furtado، نويسنده , , Kelly Silva and Salvadori، نويسنده , , Daisy Maria Fلvero and Rivelli، نويسنده , , Diogo Pineda and Barros، نويسنده , , Silvia Berlanga de Moraes and Rodrigues، نويسنده , , Maria Aparecida Marchesan and Barbisan، نويسنده , , Luis Fernando، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2009
Pages :
9
From page :
1521
To page :
1529
Abstract :
Drinking hot maté has been associated with risk for esophageal cancer in South America. Thus, the aims of this study were to evaluate the modifying effects of maté intake on DNA damage and esophageal carcinogenesis induced by diethylnitrosamine (DEN) and thermal injury (TI) in male Wistar rats. At the initiation phase of carcinogenesis, rats were treated with DEN (8 × 80 mg/kg) and submitted to TI (water at 65 °C, 1 ml/rat, instilled into the esophagus). Concomitantly, the animals received maté (2.0% w/v) for 8 weeks. Samples of peripheral blood were collected 4 h after the last DEN application for DNA damage analysis. At weeks 8 and 20, samples from esophagus and liver were also collected for histological and immunohistochemical analysis. Maté significantly decreased DNA damage in leukocytes, cell proliferation rates in both esophagus and liver and the number of preneoplastic liver lesions from DEN/TI-treated animals at week 8. A significant lower incidence of esophageal papillomas and liver adenomas and tumor multiplicity was observed in the animals previously treated with maté at week 20. Thus, maté presented protective effects against DNA damage and esophageal and liver carcinogenesis induced by DEN.
Keywords :
Maté , Diethylnitrosamine-induced esophageal and liver lesions , DNA damage
Journal title :
Food and Chemical Toxicology
Serial Year :
2009
Journal title :
Food and Chemical Toxicology
Record number :
2120996
Link To Document :
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